The discovery by Burg and Green that chloride is actively transported by the kidney's loop of Henle led to the understanding that potent diuretics such as furosemide inhibit that transport mechanism. Formidable hindrances to easy exploration of chloride inhibition directly in the kidney prompts investigation of more accessible models of chloride transport; the frog gastric mucosa and cornea. Preliminary work has disclosed that furosemide in very low concentration inhibits chloride transport, the electrical potential difference and short-circuit current of the frog gastric mucosa. This can be reversed by introduction of the HCO3/CO2 buffer pair. Treating urosemide as a weak electrolyte, the pH of media at the two surfaces of the epithelium will be varied to clarify the locus of furosemide's action. Chloride transport as a function of (HCO3), (CO2) and pH will be examined to elucidate the role of the former pair. The prime objective will be to establish the action of furosemide of the fluxes of chloride. Careful measurement of the transepithelial fluxes will allow a provisional analysis. To the extent that it is technically feasible, as many of the component plasma membrane fluxes will be acquired. This should provide a basis for understanding the action of furosemide on the chloride pump. Amphibian and mammalian gastric mucosae possess a highly efficient transport mechanism for potassium. The action loss of potassium is a major complication of furosemide therapy. Understanding developed from this proposal should advance the ultimate objective of studying the mode action of diuretics such as furosemide directly in the kidney.